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Journal Article

Rapid active zone remodeling consolidates presynaptic potentiation.

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Göttfert,  F.
Department of NanoBiophotonics, MPI for Biophysical Chemistry, Max Planck Society;

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Hell,  S. W.
Department of NanoBiophotonics, MPI for Biophysical Chemistry, Max Planck Society;

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Fulltext (public)

3032083.pdf
(Publisher version), 6MB

Supplementary Material (public)

3032083_Suppl_1.pdf
(Supplementary material), 21MB

3032083_Suppl_2.pdf
(Supplementary material), 54KB

3032083_Suppl_3.mpg
(Supplementary material), 836KB

3032083_Suppl_4.pdf
(Supplementary material), 133KB

Citation

Böhme, M. A., McCarthy, A. W., Grasskamp, A. T., Beuschel, C. B., Goel, P., Jusyte, M., et al. (2019). Rapid active zone remodeling consolidates presynaptic potentiation. Nature Communications, 10(1): 1085. doi:10.1038/s41467-019-08977-6.


Cite as: http://hdl.handle.net/21.11116/0000-0003-2269-1
Abstract
Neuronal communication across synapses relies on neurotransmitter release from presynaptic active zones (AZs) followed by postsynaptic transmitter detection. Synaptic plasticity homeostatically maintains functionality during perturbations and enables memory formation. Postsynaptic plasticity targets neurotransmitter receptors, but presynaptic mechanisms regulating the neurotransmitter release apparatus remain largely enigmatic. By studying Drosophila neuromuscular junctions (NMJs) we show that AZs consist of nano-modular release sites and identify a molecular sequence that adds modules within minutes of inducing homeostatic plasticity. This requires cognate transport machinery and specific AZ-scaffolding proteins. Structural remodeling is not required for immediate potentiation of neurotransmitter release, but necessary to sustain potentiation over longer timescales. Finally, mutations in Unc13 disrupting homeostatic plasticity at the NMJ also impair short-term memory when central neurons are targeted, suggesting that both plasticity mechanisms utilize Unc13. Together, while immediate synaptic potentiation capitalizes on available material, it triggers the coincident incorporation of modular release sites to consolidate synaptic potentiation.